Category Archives: CNS

Best Of EAST #8: Early vs Late Full Anticoagulation In TBI

Trauma professionals are always reluctant to anticoagulate TBI patients with demonstrated blood in their head. In recent years, we’ve become more comfortable providing prophylactic doses of low molecular weight heparin after a suitable period. This is typically 24-48 hours after a stable head CT in patients with select types of intracranial hemorrhage (ICH) who are at increased risk for venous thromboembolism.

But what about therapeutic dose anticoagulation in these patients? Let’s say that you have a patient with ICH who has developed a significant pulmonary embolism (PE)? Is is safe to give full dose anticoagulation? And if so, when?

The group at Shock Trauma in Baltimore attempted to answer this in one of the EAST Quick Shot presentations scheduled for this week. The did a retrospective review of 4.5 years of their own data on these patients. They specifically selected patients who had both ICH and PE and compared those who received full anticoagulation within 7 days of injury vs those who were dosed after 7 days. Outcomes studied included death, interventions for worsening ICH, and pulmonary complications.

Here are the factoids:

  • A total of 50 patients had both ICH and PE, but only the 46 who received therapeutic anticoagulation were analyzed
  • 19 patients (41%) received early anticoagulation, and 27 received it late (59%)
  • There were 4 deaths in the early group (2 from the PE, 1 from multi-system organ failure, 1 from the TBI) vs none in the late group, and this was statistically significant
  • 3 patients in the early group (18%) vs 2 in the late group (7%) had an increase in their ICH (p=0.3), and none required intervention

The authors concluded that their study failed to show any instances of clinically significant progression of ICH after anticoagulation, and that it is not associated with worse outcomes, even if started early. Thus they recommend that ICH should not preclude full anticoagulation, even early after injury.

My comment: I always say that you shouldn’t let one paper change your practice. Even a really good one. In order to ensure that you are providing the best care, more work must always be done to confirm (or refute) the findings of any provocative research. And this little Quick Shot, with little opportunity for questions from the audience, should definitely not change it!

The major issues to consider here are common ones: 

  • This was a retrospective study and it does not appear that any guideline was followed to determine who got early vs late anticoagulation. So who knows what kind of selection bias was occurring and how the surgeon decided to prescribe anticoagulation? It’s very possible that patients with a “bad CT” were put into the late group, and the not so bad ones in the early group. This would bias the results toward better outcomes in the early anticoagulation group.
  • It’s also a very small study that is extremely underpowered. The authors comment on the fact that the outcomes of the early group were not worse than the late group. However, looking at their sample size (46) shows that they would only be able to show differences if they were about 5x worse in the early group. They would realistically need about 350 total patients to truly show that the groups behaved the same. Their small numbers also preclude saying that there were no ICH progressions. There very well could have been if 300 more patients were added to the series.
  • And isn’t death a significant outcome? The authors indicated that 2 of the 4 deaths were a result of the PE. Yet there was a significant association (p=0.02) of increased death in the early anticoagulation patients that can’t be discounted.

Bottom line: It’s way too early to consider giving early anticoagulation to patients with ICH and pulmonary embolism. It may very well be shown to be acceptable, eventually. But not yet. And a much bigger prospective study will be required to confirm it.

Reference: Therapeutic anticoagulation in patients with traumatic brain injuries and pulmonary emboli. EAST Annual Assembly Quick Shot #7, 2020.

Print Friendly, PDF & Email

AAST 2019 #5: DOACs Part 2

In my last post, I reviewed a study that scrutinized reversal of direct oral anticoagulants (DOACs), and the outcomes of using various reversal agents. Today I’ll look at an abstract that compared in-hospital outcomes of elderly patients with severe TBI who were taking a variety of anticoagulant drugs, including DOACs.

The group at St. Joseph Mercy Hospital in Ann Arbor reviewed the dataset from the Michigan Trauma Quality Improvement Program database over a seven year period. To be included, patients needed to be at least 65 years old, suffer a fall, and have a significant head injury (AIS > 3). The final data consisted of records from 8312 patients treated at both Level I and II trauma centers across the state.

Here are the factoids:

  • 40% of patients were taking antiplatelet agents, 13% warfarin, 4% DOAC, and the remaining half or so were taking nothing.
  • The head injuries were severe, with mean AIS of 4.
  • After adjusting for “patient factors”, mortality or hospital outcomes were 1.6x more likely when warfarin was used
  • Complication risk increased 1.4x for warfarin and 1.3x for antiplatelet patients, but not for DOACs
  • Hospital length of stay was a day longer in the warfarin group (6.7 days) vs about 5.7 in the others

The authors concluded that elderly patients with severe TBI on DOACs fared better than those on warfarin. They stated that this could help alleviate concerns about DOACs in head trauma patients.

This is yet another interesting and surprising piece of the TBI on anticoagulants puzzle! It is obviously limited due to its retrospective database nature, which prevents us from asking even more interesting questions of this dataset. And it completely prevents us from looking at the specifics of each case including decision making, imaging, etc. But it’s a good start that should prompt us to find even better sources of data to tease out the details we must know in order to improve this patient group’s care.

Here are my questions for the presenter and authors:

  • I am very interested in the “patient factors” that were adjusted for to try to normalize the groups. Please describe in detail the specific ones that were used so we can understand how this influenced your results.
  • This information is intriguing, suggesting that warfarin is more evil that DOACs. What is the next step? What shall we do to further elucidate the problems, and how can we ameliorate the mortality and complication effects?

This is more good stuff about DOACs, and I can’t wait to hear the details.

Print Friendly, PDF & Email

Redefining Mild TBI: Who Needs To Be Transferred?

One of the more common reasons for transfer to a higher level trauma center these days is the “mild or minimal TBI.” Technically, this consists of any patient with a Glasgow Coma Scale score of 14 or 15. A transfer is typically requested for observation or neurosurgical consultation, or because the clinicians at the initial hospital are not comfortable looking after the patient.

Is this really necessary? With the number of ground level falls approaching epidemic proportions, transferring all these patients could begin to overwhelm the resources of high level trauma centers. The surgical group at Carolinas Medical Center examined their experience with a simple scoring system they designed to predict high risk minor TBI patients, and thus suitability for transfer. Here is their checklist:

Category A
  • Traumatic SAH
  • Tentorial or falcine SDH < 4mm thickn
  • Convexity SDH < 4mm thick
  • Solitary IPH < 1cm
  • Isolated intraventricular hemorrhage < 4mm
Category B
  • Any Category A lesion greater than the allowed size
  • Midline shift
  • Skull fracture
  • Compression of basal cisterns
  • Diffuse SAH or SAH involving basal cisterns
  • Subacute or chronic SDH
SAH = subarachnoid hemorrhage, SDH = subdural hemorrhage, IPH = intraparenchymal hemorrhage

Patients were considered to be low risk if they had only one or two category A lesions. If they had more than two, or any Category B lesions, they were higher risk and transfer was considered justified.

The authors retrospectively reviewed their experience with these patients over a three year period. They followed patients to see if they needed neurosurgical intervention, and evaluated the cost savings of avoiding selective transfers based on their criteria.

Here are the factoids:

  • A total of 2120 patients were studied, with 68% low risk and 32% high risk
  • Two of the low risk patients (0.14%)  ultimately required neurosurgical intervention, compared to 21% of high risk patients
  • Mean age (56), and patients taking anticoagulants or antiplatelet agents were the same in the two groups, about 2-3% for each
  • System saving by avoiding EMS transfer costs would have been $734K had the low risk patients been kept at the initial hospital

Bottom line: This study was presented as a Quick Shot paper at this year’s Eastern Association for the Surgery of Trauma meeting, so there are some key details missing. Was there an association between anticoagulation or antiplatelet agent and two failures in the low risk group? What were they, and what intervention did they require?

If this data holds up to publication, then it may provide a useful tool for deciding to keep minimal TBI patients at the local hospital. This is usually far more convenient for the patient and their family, but would require additional education of the clinicians at that hospital to help them become comfortable managing these patients. 

We use a similar tool within our Level I trauma center to decide which patients require a neurosurgical consultation. Since the low risk patients almost never require intervention, our trauma service provides comprehensive management while in hospital, and arranges for TBI clinic followup post-discharge. You can view and download a copy using the link below.

Link: Regions Hospital SAH/IPH/Skull fracture practice guideline

Reference: Redefining minimal traumatic brain injury (MTBI): a novel CT criteria to predict intervention. Quick Shot Paper #48, EAST 2019.

Print Friendly, PDF & Email

Glasgow Coma Scale For Trauma Activation: What’s The Optimal Score?

Last month, I posted a survey to  find out the Glasgow Coma Scale (GCS) values trauma centers were using to trigger their highest level trauma activation. Nearly 150 people responded, providing a nice snapshot of practices worldwide. Today, I’ll summarize the responses and provide a bit of commentary about them.

There were a total of 147 respondents from around the world. I tried to eliminate duplicates from the same center using a self-reported postal code. However, this was an optional field, so there is the possibility that a few crept in. Readers from at least six countries outside the US also responded.

The question  was: “What is the highest GCS score that triggers a top-level trauma activation at your trauma center?”

Here is a chart that shows the results. The proper way to read it is “a trauma activation is called if GCS < xx” where xx is the score under the bar in the chart.

The whole point to calling a trauma activation is to have the full trauma team and infrastructure (labs, imaging, blood, etc.) in place to rapidly assess a patient with life-threatening injuries. In theory this should afford them the best probability of survival.

So what is the optimal GCS score to activate your trauma team? Unfortunately, this remains difficult to answer exactly. From the chart, you can see that the most common scores were 8, 9, and 13. Why such a spread?

The GCS 8 and 9 levels are a no-brainer (ha!). These patients are comatose or nearly so, and obviously need prompt attention such as airway control, head CT, and neurosurgical consultation. But what about the patients with GCS 13? They have lost two points, typically for eye-opening and verbal response. This may indeed indicate  a significant head injury. But all too often we see this same score in patients who are intoxicated. Do we really need (or want) to activate the full team for each and every intoxicated patient? Can we screen them out in some way?

The answer to both questions is yes. The most important tip is to know your patient population. There is an association between GCS and need for operative intervention that was oft-quoted in the ATLS course. However, I have not been able to find a definitive paper on this topic.

I recommend that you tap into your trauma registry and create a chart that shows presenting GCS vs early neuro-intervention (ICP monitor or craniectomy within 24 hours). Find the GCS score where you see a “significant” bump in the number needing a procedure, and use this as your trauma activation threshold. This report will automatically take into account the number of intoxicated patients you treat.

I would also recommend you do a separate report on age vs need for neuro-intervention with GCS<15. The older population tends to require craniectomy for TBI more often and at higher GCS levels than younger people. You may factor this into your single GCS criterion, or add a separate one at a different level for patients over 55, or 60, or whatever reflects your patient age mix.

Bottom line: Make sure your GCS trauma activation criteria adequately identify your patients who truly have a need for speed in their trauma evaluation. A GCS of 8 or 9 may be too low, and a score in the teens is probably more appropriate for most centers. Use your trauma registry to determine the best score for you so you can capture the patients who have critical needs while trying to keep overtriage under control.

 

Print Friendly, PDF & Email

GCS At 40: The New GCS-40

As discussed in my first post in this series, the original Glasgow Coma Scale (GCS) was described in 1974. It was originally intended to be a chart of all three components, trended over time. Ultimately, the three values for eye opening, verbal, and motor responses were combined into a single score ranging from 3-15. This combined score has become the main focus of our attention, with less interest in the individual components.

Here is the original GCS:

Forty years later (2014), there was interest in tweaking it to overcome a few of the perceived shortcomings. Two relatively small changes were made. First, a few terminology changes were made in the eye opening and verbal response components. Eye opening was clarified to indicate opening to pressure, not pain, and speech, not sound. Verbal response was also clarified, changing “incomprehensible” to “sounds”, and “inappropriate” to “words.”

Additionally, when eye opening or verbal response could not be tested (swelling, intubation), the value was scored as a 1. This was changed in 2014, so that the non-testable components are now marked “NT” and the total score should not be calculated.  Here’s an example:

  • Original GCS: E1 V1T M3 = 5T
  • GCS-40: E1 V-NT M3   (no total)

Here’s the new GCS-40 description published in 2014:

Finally, this year Teasdale and associates added one final tweak. They incorporated an indicator of pupillary response. This table shows the levels of response:

This factor is subtracted from the GCS-40, now resulting in score that can range from 1-15. Addition of this component greatly improves our ability to predict outcome.

Why does all this matter? One important reason is that the American College of Surgeons Trauma Quality Improvement Program will begin accepting data in 2019 with GCS 40 data. The National Trauma Databank data definitions will also incorporate GCS 40 in next tear. It looks like there will be a phase-in period where either system can be used. I could not find any indication that the pupillary score would be included any time soon.

I’m sure research will continue on this staple of trauma evaluation. Expect more tweaks in the future as we try to improve our ability to follow our patients clinically and predict how well they will do.

Print Friendly, PDF & Email